Guizani Imen, Fourti Nesrine, Zidi Wiem, Feki Moncef, Allal-Elasmi Monia
LR99ES11, Laboratory of Biochemistry, Department of Biochemistry, Faculty of Medicine, La Rabta Hospital, University of Tunis El Manar, Jebbari, 1007, Tunis, Tunisia.
Faculty of Mathematics, Physics and Natural Sciences, University of Tunis El Manar, Tunis, Tunisia.
Inflamm Res. 2021 Aug;70(8):847-858. doi: 10.1007/s00011-021-01487-6. Epub 2021 Jul 20.
Recognizing only sharp elevation in a short period of time, the COVID-19 SARS-CoV-2 propagation is more and more marked in the whole world. Induced inflammation afterwards infection engenders a high infiltration of immune cells and cytokines that triggers matrix metalloproteinases (MMPs) activation. These endopeptidases are mediators of the lung extracellular matrix (ECM), a basic element for alveoli structure and gas exchange.
When immune cells, MMPs, secreted cytokines and several other mediators are gathered a pathological matrix remodeling occurs. This phenomenon tends to tissue destruction in the first place and a pulmonary hypertrophy and fibrosis in the second place.
After pathological matrix remodeling establishment, pathological diseases take place even after infection state. Since post COVID-19 pulmonary fibrosis is an emerging complication of the disease, there is an urge to better understand and characterize the implication of ECM remodeling during SARS-CoV-2 infection.
Targeting MMPs and their inhibitors could be a probable solution for occurred events since there are many cured patients that remain with severe sequels even after the end of infection.
仅在短时间内就迅速传播，新型冠状病毒肺炎（COVID-19）严重急性呼吸综合征冠状病毒2（SARS-CoV-2）在全球的传播愈发显著。感染后引发的炎症导致免疫细胞和细胞因子大量浸润，进而触发基质金属蛋白酶（MMPs）的激活。这些内肽酶是肺细胞外基质（ECM）的介质，而肺细胞外基质是肺泡结构和气体交换的基本要素。
当免疫细胞、MMPs、分泌的细胞因子和其他几种介质聚集时，就会发生病理性基质重塑。这种现象首先倾向于组织破坏，其次会导致肺肥大和纤维化。
病理性基质重塑形成后，即使在感染状态结束后仍会出现病理性疾病。由于COVID-19后肺纤维化是该疾病新出现的并发症，因此迫切需要更好地了解和描述SARS-CoV-2感染期间ECM重塑的影响。
针对MMPs及其抑制剂可能是应对已发生情况的一种解决方案，因为有许多康复患者即使在感染结束后仍留有严重后遗症。
